A Stroke Alert Protocol Decreases the Time to Diagnosis of Brain Attack Symptoms in a Pediatric Emergency Department.

OBJECTIVE: To determine whether a stroke alert system decreases the time to diagnosis of children presenting to the emergency department (ED) with acute-onset focal neurologic deficits. STUDY DESIGN: We performed a retrospective comparison of clinical and demographic information for patients who presented to the ED of a tertiary children's hospital with acute-onset focal neurologic deficits during the 2.5 years before (n = 14) and after (n = 65) the implementation of a stroke alert system. The primary outcome was the median time to neuroimaging analyzed using a Wilcoxon rank-sum test. RESULTS: The median time from ED arrival to neuroimaging for patients with acute-onset focal neurologic deficits decreased significantly after implementation of a stroke alert system (196 minutes; IQR, 85-230 minutes before [n = 14] vs 82 minutes; IQR, 54-123 minutes after [n = 65]; P < .01). Potential intravenous tissue plasminogen activator candidates experienced the shortest time to neuroimaging after implementation of a stroke alert system (54 minutes; IQR, 34-66 minutes [n = 13] for intravenous tissue plasminogen activator candidates vs 89.5 minutes; IQR, 62-126.5 minutes [n = 52] for non-intravenous tissue plasminogen activator candidates; P < .01). CONCLUSIONS: A stroke alert system decreases the median time to diagnosis by neuroimaging of children presenting to the ED with acute-onset focal neurologic deficits by more than one-half. Such a protocol constitutes an important step in ensuring that a greater proportion of children with arterial ischemic stroke are diagnosed in a time frame that enables hyperacute treatment.

Placental Pathology in Neonatal Stroke: A Retrospective Case-Control Study.

OBJECTIVE: To assess the association of placental abnormalities with neonatal stroke. STUDY DESIGN: This retrospective case-control study at 3 academic medical centers examined placental specimens for 46 children with neonatal arterial or venous ischemic stroke and 99 control children without stroke, using a standard protocol. Between-group comparisons used χ2 and Fisher exact t test. Correlations used Spearman correlation coefficient. RESULTS: Case placentas were more likely than controls to meet criteria for ≥1 of 5 major categories of pathologic abnormality (89% vs 62%; OR, 5.1; 95% CI, 1.9-14.0; P = .0007) and for ≥2 categories (38% vs 8%; OR, 7.3; 95% CI, 2.9-19.0; P < .0001). Fetal vascular malperfusion occurred in 50% of cases and 17% of controls (OR, 4.8; 95% CI, 2.2-10.5; P = .0001). Amniotic fluid inflammation occurred in 46% of cases with arterial ischemic stroke vs 25% of controls (OR, 2.6; 95% CI, 1.1-6.1; P = .037). There was evidence of a "stress response" (meconium plus elevated nucleated red blood cells) in 24% of cases compared with 1% of controls (OR, 31; 95% CI, 3.8-247.0; P < .0001). CONCLUSIONS: Placental abnormality was more common in children with neonatal stroke compared with controls. All placental findings represent subacute-to-chronic intrauterine stressors. Placental thrombotic processes were associated with both arterial and venous stroke. Our findings provide evidence for specific mechanisms that may predispose to acute perinatal stroke. Amniotic fluid inflammation associated with neonatal arterial ischemic stroke deserves further investigation.

Safety and retention rate of rufinamide in 300 patients: a single pediatric epilepsy center experience.

OBJECTIVE: Reports of studies evaluating rufinamide as an add-on therapy in children and adolescents with refractory epilepsy are restricted to a few publications. Prospective multicenter studies including children and adults have yielded important information about several types of epilepsies and syndromes. We evaluated the use of rufinamide in a single pediatric center with a large cohort and long-term follow-up period. METHODS: We retrospectively included patients taking rufinamide from November 2008 to March 2013. Response was defined by a seizure reduction of ≥50% compared to baseline. RESULTS: Three hundred patients with a median age of 9.1 years (range 0.4-29.6 years) were reviewed. Median follow-up was 9 months (range 1-37 months). Epilepsy etiology was classified as genetic (23.7%), structural/metabolic (41%), and unknown cause (35.3%). Overall, rufinamide treatment led to a median seizure frequency reduction of 59.2% from responders to baseline. Seizure reduction was greater in patients with genetic etiology compared to structural/metabolic (66.2% vs. 45.5% responders, p = 0.005). Rufinamide was discontinued in 110 (36.7%) of 300 patients: 63 (21%) due to unsatisfactory response, 47 (15.7%) due to side effects, and in 18 (6%) of those due to both. Most common adverse effects were sleepiness, vomiting, mood changes, nausea, and loss of appetite. Median time to loss of efficacy was 11.6 months (range 3-28 months). SIGNIFICANCE: Rufinamide provides satisfactory seizure reduction as an adjunctive treatment in refractory epilepsy. Results need to be interpreted in the setting of data acquisition, including inherent biases of retrospective studies. Patients with a known genetic etiology may have better responses than patients with structural/metabolic etiology.